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80 Cards in this Set

  • Front
  • Back
What are some mechanisms of actions of corticosteroids important for treating inflammatory skin dz?
inhibit transcription of cytokines, COX-2, vascular adhesion mols, transcription factors, iNOS, PLA2

neutrophils: neutrophilia, inhibit migration
lymphocytes: lymphopenia (T cells), redistribution, ↓ activation
eosinophils: inhibit migration
What factors are important in long term corticosteroid therapy?
select intermediate acting corticosteroid
taper to lowest effective dose
administer on EOD schedule to minimize side effects
after long term therapy, it may take longer for adrenal gland recovery --> withdrawal syndrome may be observed in animals after glucocorticoids are discontinued
What is the dose of corticosteroids in dogs for:

a. physiologic
b. anti-inflammatory
c. immunosuppressive
d. membrane stabilizing
a. 0.25 mg/kg
b. 1.0 mg/kg
c. 2.0 mg/kg
d. 30 mg/kg
What are some differences in cats & horses vs. dogs when using corticosteroids?
cats often require higher doses than dogs possibly d/t differences in receptors

cats, horses: prednisolone preferred over prednisone
-either do no absorb prednisone orally well or once it is absorbed, there is a deficiency in ability to convert to prednisolone

cats are more resistant to adverse effects than dogs

repository forms of methylprednisolone acetate (Depo-Medrol) have been administered to cats: slowly absorbed over ~3 weeks
What are some adverse effects of corticosteroids with regard to the following body systems:

a. endocrine
b. musculoskeletal
c. GI
a. HPA axis suppression, ↓ conversion of T4 --> T3, anti-insulin effects
b. ↓ collagen synthesis, osteoporosis, myopathy, laminitis (horses)
c. ↑ risk of GI ulceration, diarrhea, ↑ risk of pancreatitis
What are some adverse effects of corticosteroids with regard to the following body systems:

a. immune system
b. CNS
c. metabolic
d. renal
a. ↓ immune response, ↓ wound healing, ↑ risk of infection
b. polyphagia, euphoria, restlessness, behavior changes
c. hyperlipidemia, protein catabolism, steroid hepatopathy (dogs)
d. PU/PD, recurrent UTIs (d/t ↓ immune response & PU/PD), sodium & water retention
In what patients should you use caution in treating w/ steroids?
patients w/ DM, renal dz, GI dz, young growing animals, pregnant animals, animals requiring tissue healing (ex. surgical patients), patients on NSAIDs (don't give steroids)
What are some clinical uses of omega fatty acids?
pruritic dermatitis, arthritis, ulcerative colitis
What is proposed mechanism of action of fatty acid supplements?
arachadonic acid (a n-6 FA) --> COX & LOX --> inflammatory prostaglandins & leukotrienes (PG2, LT4 series)

FA supplements believed to compete w/ arachadonic acid for COX &/or LOX
•n-3 FAs are either incapable of further metabolism to inflammatory mediators or are metabolized to less inflammatory mediators (PG3, LT5 series)
Which antihistamines are used to tx inflammatory skin conditions in dogs & cats?
1st generation antihistamines: chlorpheniramine, diphenhydramine, hydroxyzine
What are the pharmacological actions of antihistamines used to tx inflammatory skin dz?
anti-inflammatory (antihistamine)
sedation (H1 blocking effect)
appetite stimulation
antimuscarinic effects (atropine-like): dry mouth, urinary retention
What are the clinical effects of using antihistamines for tx of inflammatory skin dz?
variable success in controlling pruritis & skin inflammation in animals
some drugs not absorbed in dogs
more effective when combined w/ corticosteroids (can use lower steroid dose)

a. drug class
b. mechanism of action
c. clinical uses in horses
d. clinical uses in dogs
e. reason why not used frequently
a. methylxanthine

b. non-specific phosphodiesterase (PDE) inhibitor
-phosphodiesterases hydrolyze cyclic AMP to 5’-nucleotide monophosphates
-cyclic AMP important messenger that suppresses inflammation in cells in tissues
-blocking PDE --> ↑ cyclic AMP --> anti-inflammatory effects, improved blood flow, inhibition of cytokine production

c. navicular dz, laminitis, sepsis, endotoxemia
d. vasculitis, contact dermatitis, dermatomyositis, atopic dermatitis
e. has to be given q8h
What are the pharmalogical actions of cyclosporine?
-more specific for T cells than B cells
-suppresses IL-2 (which normally activates T cells) & other cytokines
-blocks proliferation of activated T lymphocytes
-suppresses mast cell release
-does NOT cause significant myelosuppression or suppress nonspecific immunity
What are some common clinical uses of cyclosporine?
-suppression of immunity for organ transplantation
-atopic dermatitis
-canine perianal fistulas
-immune mediated dz
-eosinophilic granuloma complex (cat)
-feline asthma
-KCS: topical tx
-other uses: IBD, granulomatous meningoencephalitis, sebaceous adenitis, idiopathic sterile nodular panniculitis, IMHA
What are some pharmacokinetic issues associated w/ Atopica (vet formulation of cyclosporine)?
oral absorption in dogs is highly variable (20-30%)
-better absorption if given w/o food, but ↑ incidence of vomiting

intestinal metabolism by cytochrome P-450 (CYP) enzymes & efflux caused by intestinal p-glycoprotein (pumps absorbed drug back into SI --> eliminated) account for most of loss in systemic availability after oral administration
-CYP inhibitors such as ketoconazole, diltiazem can inhibit pre-systemic metabolism of cyclosporine --> profound ↑ in systemic availability
-can be used clinically to ↓ required dosage of cyclosporine & thus save money
What are some adverse effects of cyclosporine?
nausea, anorexia, vomiting, shedding of hair, replaced by softer, glossier coat

less common: papillomas (dogs), gingival hyperplasia (dogs), toxoplasmosis (cats), tremors, convulsions, nephrotoxicitiy
What are the immunosuppressive actions of glucocorticoids?
lymphopenia: primarily T cells

↓ MP function & production of cytokines

suppression of cell mediated (T cell) immunity

few direct effects on B cells

a. mechanism of action
b. clinical uses
a. alkylate bases of DNA --> cross-links bases of DNA --> cessation of DNA synthesis --> cell death
-cytotoxic effect on lymphocytes: B cells effected more than T cells
-can be used in combo w/ steroids that primarily work against T cells

b. IMHA, immune mediated skin dz (ex. pemphigus foliaceus), systemic lupus, immune mediated joint dz (RA), cancer chemo (LSA)

a. mechanism of action
b. clinical uses
a. metabolized to active form 6-mercatopurine (6-MP)
-interferes w/ lymphocyte proliferation b/c it inhibits de novo synthesis of purines, which is critically important for activated lymphocytes
-activated T cells most affected
b. immune mediated skin dz, IMHA, IMTP, IBD, immune mediated arthritis (RA), graft rejection, acquired myasthenia gravis

a. pharmacokinetics
b. adverse effects
c. problems in cats
a. onset of effects: 3-5 weeks
-long term therapy: administered EOD w/ prednisolone given on the alternate days
b. idiosyncratic bone marrow suppression --> serious leucopenia, thrombocytopenia (monitor CBC continuously during therapy)
-GI: vomiting, diarrhea (may be transient)
-hepatotoxicosis: rare
-pancreatitis: when given in combo w/ steroid (not well documented)
c. more susceptible to toxicity than dogs
-cats are deficient in TPMT, enzyme that converts 6-MP to non-toxic 6-MP nucleotides
-can produce profound bone marrow suppression (neutropenia) in cats if used at dog dose --> if used, dose should be much lower
What drug classes can be used as anti-emetics?
serotonin antagonists
NK-1 receptor blockers

a. mechanisms of action for tx of vomiting
b. adverse effects
c. drugs in class
a. broad spectrum
-anti-dopaminergic: main effect
-block α-1 receptors in vomiting center
-some may also block histamine & muscarinic receptors
b. sedation, ataxia, α-adrenergic block (hypotension), altered involuntary muscle activity (extrapyramidal signs; rare), seizures
c. chlorpromazine, acepromazine

a. drugs in class
b. mechanisms of action for tx of vomiting
c. adverse effects
a. atropine, scopolamine, aminopentamide (centrine)
b. block Ach at muscarinic receptors --> inhibit vomiting from vestibular stimulation & CRTZ
c. xerostomia (dry mouth), ↓ stomach emptying, ileus, constipation, urine retention

a. drugs in class
b. mechanisms of action for tx of vomiting
c. adverse effects
a. chlorpromazine, diphenhydramine
b. blocks H1 receptor --> weak antiemetic effects
-histaminic nerve transmission stimulates vomiting from CRTZ, but this effect is apparently more prominent in dogs than cats
c.sedation, antimuscarinic effects, excitement (cats)
metoclopramide: mechanisms of action for tx of vomiting
inhibits dopaminergic transmission in CNS

↑ emptying of stomach & upper duodenum

inhibits serotonin receptors (at high doses)
serotonin antagonists

a. example drug
b. clinical use for tx of vomiting
a. ondanesetron

b. most often used an antiemetic in cancer chemotherapy: very expensive
How is dexamesthasone used as a tx for vomiting?
dec. GI inflammation: sometimes used in combo w/ other drugs to tx vomiting caused by cancer chemo
NK-1 receptor blockers

a. example drug
b. mechanisms of action
c. clinical uses
d. adverse effects
a. Maropitant
b. antagonizes neurokinin (substance P): potent emetic at vomiting center & perhaps CRTZ
-blocks vomiting induced from central & peripheral stimuli
c. used primarily with drugs known to be highly emetic (ex. cancer chemo)
d. none reported
What drugs are used for tx of motion sickness in:

a. dogs
b. cats
a. antihistamines, NK-1 blockers
b. phenothiazines
What drugs can be used to tx vomiting caused by drugs?
choose drug that ↓ activity in CRTZ
ex. phenothiazines, metoclopramide, serotonin blockers, NK-1 blockers
What are the common clinical uses of GI pro-kinetic agents?
post-op ileus (horses), GI motility disorders, gastroparesis (dogs), ↑ rumen motility, ↑ colon motility (cats, horses)
What are 4 drugs commonly used as GI pro-kinetic agents?

a. mechanism of action
b. pharmacologic effects
a. dopamine (D2) antagonist, serotonin (5-HT4: stimulatory) agonist), serotonin (5-HT3: inhibitory) antagonist: at high doses
-proposed mechanisms: ↑ release of Ach in GI tract, ↑ sensitivity to Ach, antagonism of dopamine’s inhibitory action on GI motility
b. ↑ tone of gastroesophageal sphincter
-relaxes pyloric sphincter
-↑ stomach emptying
-↑ motility in proximal SI (little action in distal GI tract)

a. clinical uses in small animals
b. clinical uses in large animals
c. adverse effects
a. antiemetic, ↑ stomach emptying
b. ↑ intestinal motility, ↑ rumen motility
-of little benefit to tx intestinal ileus in horses b/c it doesn’t stimulate colon
c. antidopamine effects: sedation, involuntary muscle movements, ↓ seizure threshold
-behavior changes, excitement: horses

a. mechanism of action
b. pharmacologic effects
a.serotonin (5-HT4) agonist, serotonin (5-HT3) antagonist, may enhance release of Ach at myenteric plexus
-in cats: may directly stimulate smooth muscle motility via an unknown noncholinergic mechanism
b. stimulates or restores motility along entire length of GI tract
-coordinated motility stimulation
-↓ esophageal reflux
-↑ stomach emptying
-↑ intestinal motility
-↑ colonic motility

a. clinical uses in small animals
b. clinical uses in horses
a. gastroesophageal reflux, ↑ stomach emptying, post-op ileus, constipation & megacolon
b. ↑ bowel motility, post-op ileus (not used much anymore: no IV form)

a. mechanism of action as GI pro-kinetic agent
b. pharmacologic effect
c. adverse effects
a. ↑ activation of motilin receptors (low doses)
b. ↑ gastric emptying (does not effect distal GI tract)
-NOT drug of choice b/c it fails to restore normal motility pattern
c. can cause diarrhea in horses thru effect on normal intestinal flora

a. pharmacologic effects
b. clinical use in horses
a. ↓ sympathetic tone
-direct excitatory effects on intestinal smooth muscle
-inhibition of pain stimulus
b. IV infusion for tx of post-op ileus
What drugs/drug classes are used to tx &/or prevent GI ulcers?
H-2 blockers
proton pump inhibitors

a. example drugs
b. mechanism of action
c. adverse effects
d. drug interactions
a. magnesium hydroxide (Milk of Magnesia), calcium carbonate (Tums), aluminum hydroxide (Amphogel)
b. neutralize stomach acid to form water & neutral salt
-may stimulate local prostaglandin synthesis
c. not absorbed --> lack serious systemic effects
-diarrhea, constipation, alkalosis at high doses
d. cations interfere w/ drug absorption: fluoroquionolones, tetracyclines
-↑ stomach pH can interfere w/ drug absorption: ketoconazole, itraconazole
H-2 blockers

a. drugs in class
b. mechanism of action
c. clinical uses
a. cimetidine, ranitide, famotidine
b. block histamine H2 receptor on gastric parietal cell --> inhibit gastric acid secretion, ↑ gastric pH
c. gastritis, gastric ulcers, duodenal ulcers, GI ulcer prevention, esophagitis, mast cell tumors, hypergastrinemic syndromes
-ranitidine most commonly used in horses: better oral absorption
H-2 blockers

a. adverse effects
b. drug interactions
c. miscellaneous effects
a. good safety record
b. cimetidine inhibits CYP-450 enzymes --> inhibits clearance of some drugs (others less likely to cause such a rxn)
c. stimulate intestinal smooth muscle: ranitidine, nizatidine
-anti-cholinesterase action --> ↑ gastric emptying, ↑ colonic motility
-clinical benefits uncertain

immunologic effects: not well established
-cimetidine can block H2 receptors on suppressor T cells --> ↑ lymphocyte responses to mitogen stimulation

-cytoprotection in GI tract: cimetidine may strengthen gastric mucosal defenses against ulceration by ↑ bicarb secretion

a. mechanism of action
b. side effects
c. clinical use
d. drug interactions
a. dissociates in acid milieu of stomach to sucrose octasulfate & aluminum hydroxide
-creates a protective effect by binding to ulcerated mucosa --> prevents back diffusion of H+ ions & inactivates pepsin
-↑ local synthesis of prostaglandins
b. not absorbed systemically: virtually free of side effects
c. prevention & treatment of gastric & intestinal ulceration
-little evidence of efficacy for preventing NSAID induced ulcers
d. aluminum may inhibit absorption of some drugs (ex. fluoroquionolones, tetracyclines)
proton pump inhibitors

a. example drug
b. mechanism of action
c. acid suppression & efficacy
a. omeprazole (Prilosec)
b. inhibit H+/K+ proton pump at luminal surface of gastric parietal cell --> inhibits secretion of H+ ions into stomach lumen
c. very potent acid suppressing drugs (10-20x cimetidine) w/ long lasting effects (~24 hrs)
-weak bases that favor accumulation in acid environment of parietal cells
-may be delayed onset before they achieve maximum efficacy
-superior to other antisecretory drugs for tx of NSAID induced ulcers
-inhibitory effect against Helicobacter
proton pump inhibitors

a. clinical uses in dogs
b. clinical uses in horses
c. drug interactions
a. used in dogs that need potent, long acting acid suppression, dogs w/ NSAID induced ulcers, or dogs that fail to respond to other anti-ulcer drugs
b. treatment & prevention of ulcers (OTC formulation available: UlcerGuard)
c. ↑ gastric pH may ↓ oral absorption of some drugs (ex. ketoconazole, itraconazole)

a. mechanism of action
b. clinical uses
c. adverse effects
a. synthetic PGE-1 analog
b. prevention of NSAID induced ulcers (not as useful for treating existing ulcers)
c. abdominal discomfort, mild vomiting, diarrhea, do NOT use in pregnant animals
What are some roles of prostaglandins in the GI tract?
-protection of GI mucosa
-stimulation of protective mucus & bicarbonate secretion
-stimulation of blood flow
-anti-inflammatory effects
-stimulation of cell turnover & repair
What are some tx regimens for Helicobacter gastritis?
2 drug combinations: bismuth + AB, omeprazole + AB

3 drug combinations: bismuth + 2 AB’s, omeprazole + 2 AB’s

ABs: Metronidazole, Amoxicillin, Clarithromycin
What drugs/drug classes are used to tx diarrhea?
kaolin-pectin formulations
bismuth subsalicylate
kaolin-pectin formulations

a. mechanism of action
b. effectiveness
a. binding of bacterial toxins in GI tract (proposed)

b. clinical studies have failed to show benefit from use
may change consistency of stools, but will not ↓ fluid or electrolyte loss, nor will it shorten duration of illness
bismuth subsalicylate

a. effects of bismuth
b. effects of subsalicylate
a. may have some ability to adsorb bacterial endotoxins, anti-Helicobacter effect
b. anti-inflammatory (some PGs mediate secretory diarrhea)
-active ingredient: absorbed systemically

a. drugs in class
b. mechanism of action for tx of diarrhea
c. why are they rarely used?
a. atropine, scopolamine, buscopan
b. block Ach at muscarinic receptors --> inhibits smooth muscle tone in intestines, inhibits intestinal secretions
c. questionable efficacy for most diarrhea seen in vet med (few cases are classified as “hypermotile”)
-intestinal motility is already impaired in some patients w/ diarrhea & these drugs may worsen diarrhea by creating a “stove pipe” effect
-adverse effects: ileus, xerostomia, urine retention, cycloplegia, tachycardia, CNS excitement
N-butylscopolammonium bromide (Buscopan)

a. drug class
b. clinical use
a. antimuscarinic
b. registered for tx of spasmodic colic in horses
-do not use in colic caused by impaction

a. example drug used to tx diarrhea
b. effects on GI tract
c. adverse effects
a. loperamide (Imodium)
b. GI effects: ↑ tone of sphincters (intestinal, biliary), ↑ segmental tone, ↓ propulsive activity, ↑ water absorption
c. contraindicated in infectious diarrhea b/c may significantly slow GI transit time & ↑ absorption of bacterial toxins

few CNS effects: membrane pump p-glycoprotein helps remove drug
-dogs that are deficient in p-glycoprotein (ex. Collies) may be prone to toxicity

a. drug class
b. clinical use in tx of diarrhea
a. macrolide AB
b. chronic diarrhea in dogs w/ unknown etiology
-large & small intestines may be affected
-diarrhea may be caused by bacteria & has an inflammatory component
-treated animals respond quickly to tx (< 3 d) & relapse quickly when therapy is discontinued
metronidazole: clinical use in tx of diarrhea
used to tx chronic diarrhea caused by GI protozoa (ex. Giardia), anaerobic bacteria

ant-inflammatory effect: ↓ cell mediated immune response
What antimicrobials are used to tx diarrhea in calves?
oral amoxicillin x 3d. or systemic ceftiofur

a. metabolism
b. effects on GI tract
c. clinical use
d. adverse effects
a. prodrug: combination of sulfapyridine & 5-aminosalicylic acid (mesalamine)
-broken down by bacteria in colon to release 2 drugs
-sulfonamide component absorbed into circulation
-salicylic acid component remains active in GI tract
b. salicylate component: ↓ PGs, LTs, ↓ IL-1, oxygen radical scavenging activity
c. drug of choice for initial tx of ulcerative or idiopathic colitis, or plasmacytic-lymphocytic colitis after dietary therapy has been attempted
d. sulfonamide component is absorbed & can produce adverse effects in some animals, such as KCS in dogs
-cannot use in patients that have allergic rxns to sulfonamides

a. drug class
b. clinical uses
a. locally acting corticosteroid
b. limited use for tx of diarrhea in dogs & cats
-coated tablet: coating does not release drug until pH > 5.5 (distal GI tract)
-if any is absorbed, 80-90% inactivated by 1st pass metabolism: systemic steroid side effects minimal

a. drugs used as antitussives
b. mechanism of action
hydrocodone: most often used in vet med
-similar to codeine in action, but more potent
-combined w/ an anticholinergic drug (homatropine) in Hycodan: added to discourage abuse
-efficacy has not been established in animals
dextromorphan: not a true opiate
-suppresses medullary cough center
-lacks opiate receptor effects: analgesia & addiction
-antitussive efficacy questionable
-poor absorption in dogs
butorphanol: µ antagonist, κ agonist
-potent antitussive
-poorly bioavailable: oral dose higher than IV or SQ dose
-high doses may induce side effects such as sedation
b. directly depress cough center in medulla w/o binding to traditional opiate receptors
What are the pharmacologic effects of B-2 agonists used as bronchodilators?
relax airway smooth muscle
relieve bronchoconstriction
inhibit release of mediators from mast cells
↑ mucociliary clearance: significance unknown
How is epinephrine used to tx respiratory dz?
drug of choice for emergency tx of life-threatening bronchoconstriction

a. drug class
b. clinical use
a. B-2 agonist
b. most commonly used β-2 agonist in small animals (lasts longest)
-long acting: 6-8 hours
-not absorbed after oral administration in horses

a. drug class
b. clinical use
c. adverse effects
d. restrictions to use
a.partial B-2 agonist
b. tx of choice for heaves (RAO) in horses
c. sweating, muscle tremors, restlessness, tachycardia
d. use illegal in food animals
-β-2 agonists have been used as repartitioning agents: repartitions nutrients away from adipose tissue in favor of muscle
-residues pose threat to people (pregnant women, people w/ heart conditions)
What are some adverse effects of B-2 agonists?
excitement, muscle tremors, hyperthermia, tachycardia, ventricular arrhythmias, tolerance w/ chronic use
theophylline, aminophylline

a. drug class
b. mechanism of action
a. methyxanthines
b. non-specific phosphodiesterase (PDE) inhibitor
-phosphodiesterases hydrolyze cyclic AMP to 5’-nucleotide monophosphates
-cyclic AMP important messenger that suppresses inflammation in cells in tissues
blocking PDE --> ↑ cyclic AMP --> inhibits release of inflammatory mediators from mast cells, anti-inflammatory effects, bronchial smooth muscle relaxation
-improve diaphragmatic strength, ↑ mucociliary clearance
theophylline, aminophylline

a. clinical uses in SA
b. clinical uses in horses
c. adverse effects
a. bronchoconstrictive airway dz, collapsing trachea, allergic bronchitis, COPD
b. heaves (RAO): not used much d/t narrow therapeutic index & incidence of adverse effects (excitement, tachycardia)
c. ↑ risk of arrhythmias, excitement, tremors, ↑ risk of seizures, vomiting, nausea
What corticosteroids are commonly used to tx respiratory dz in:

a. dogs
b. cats
c. horses
a. oral prednisone/prednisolone is usually drug of choice
b. oral prednisolone, IM methylprednisolone acetate (Depo-Medrol)
c. dexamethasone, prednisolone
What are the clinical uses of corticosteroids in respiratory dz?
bronchoconstrictive dz, heaves (RAO), allergic bronchitis, feline asthma, COPD, airway inflammation

a. drug class
b. adverse effects
c. species used in
a. inhaled corticosteroid
b. minimal systemic adverse effects: significant 1st pass effects prevent systemic blood concentrations if it is swallowed after delivery
c. cats, horses

a. behavior drugs in class
b. mechanisms of actions
c. clinical uses
a. diazepam, alprazolam (Xanax)
b. activate benzodiazepine receptors in CNS, facilitate GABA (inhibitory neurotransmitter) in CNS
c. fears & phobias, anxiety (urine spraying)

a. mechanism of action
b. clinical uses
c. adverse effects
d. additional considerations
a. serotonergic & dopaminergic mechanisms
b. urine spraying, separation anxiety, thunderstorm phobia (numerous uses)
c. GI (uncommon)
d. may require 1-3 weeks to take effect
-no potential for abuse
tricyclic antidepressants

a. drugs in class
b. mechanism of action
c. clinical uses
a. clomipramine, amitriptyline
b. block uptake of serotonin & norepi
c. control of aggression, urine spraying, anxiety, hypervocalization, compulsive disorders
tricyclic antidepressants

a. adverse effects
b. additional considerations
a. anticholinergic (dry mouth, urinary/fecal retention), sedation
b. bitter taste
-may require 2-4 weeks to take effect
-contraindicated w/ cardiac conduction abnormalities, seizures
-not recommended for breeding males
-OD potential for pets & humans: no antidote
-metabolized by CYP 450 enzymes: concurrent use of cimetidine, etc. --> high serum concentrations of TCA
selective serotonin reuptake inhibitors

a. drugs in class
b. mechanism of action
c. clinical uses
a. fluoxtine (Prozac), paroxetine (Paxil)
b. blocks reuptake of serotonin
c. separation anxiety, urine spraying, compulsive disorders, aggression
selective serotonin reuptake inhibitors

a. adverse effects
b. additional considerations
a. anorexia, nausea, diarrhea, anxiety, irritability, insomnia
b. fluoxetine: may require 3-4 weeks to take effect
-gradually ↑ dose over 2 weeks to ↓ side effects
monoamine oxidase-B inhibitors

a. example drug
b. mechanism of action
c. clinical uses
d. drug interactions
a. selegiline (Anipryl)
b. irreversibly inhibit monoamine oxides, inhibit catabolism of catecholamines (esp. dopamine)
c. cognitive dysfunction & sleep disorders in dogs
d. risk of serious drug interactions, esp. w/ TCAs, SSRIs, other MAOIs (ex. amitraz)

a. side effects
b. additional considerations
a. sedation, ataxia, muscle relaxation, polyphagia, paradoxical excitation, memory deficits, idiosyncratic hepatic necrosis in cats given oral diazepam (rare), discontinuation rxns
b. may disinhibit aggressive behavior
-rapid onset of action
-short T1/2 in dogs
-after chronic use, withdrawal gradually to avoid discontinuation syndrome
What conditions is clomipramine registered for?
approved for tx of separation anxiety of dogs in US & for tx of compulsive disorders in Canada